Systems and methods for delivering electric current for spinal cord stimulation

ABSTRACT

Various system embodiments comprise a lead having a distal end and a proximal end. The distal end includes a plurality of electrodes. The lead is configured to be fed into a dorsal epidural space of a human to a desired region of a spinal column and to be fed laterally to at least partially encircle a spinal cord in the desired region to place at least one stimulation electrode in position to stimulate a dorsal nerve root and at least another stimulation electrode in position to stimulate a ventral nerve root. The desired region may include cervical vertebrae, thoracic vertebrae, or lumbar vertebrae. Some embodiments stimulate the spinal cord in the T1-T5 region.

CROSS REFERENCE TO RELATED APPLICATIONS

This application claims the benefit of U.S. Provisional Application No.61/048,736, filed on Apr. 29, 2008, under 35 U.S.C. § 119(e), which ishereby incorporated by reference.

The following commonly assigned U.S. patent application is related andis incorporated by reference in its entirety: “Systems and Methods ForSelectively Stimulating Nerve Roots,” Ser. No. 61/048,742 (AttorneyDocket 279.G34PRV), filed Apr. 29, 2008.

TECHNICAL FIELD

This application relates generally to medical devices and, moreparticularly, to systems, devices and methods for delivering electrodesfor spinal cord stimulation.

BACKGROUND

Sympathetic over activation is involved in a variety of cardiovasculardisease, such as ventricular arrhythmias, myocardial infarction (MI),heart failure (HF), etc. Therapies that are based on autonomicmodulation have shown efficacy in a variety of cardiovascular diseasesin both preclinical and clinical studies. The autonomic balance can bemodulated to have more parasympathetic tone by stimulatingparasympathetic targets or inhibiting sympathetic targets, and can bemodulated to have more sympathetic tone by stimulating sympathetictargets or inhibiting parasympathetic targets.

Spinal cord stimulation has been proposed for a variety of treatments,such as pain control. One known system for delivering electricalstimulation to neural targets in and around the spinal cord uses a leadinserted one-dimensionally into the dorsal epidural space of the spinalcord.

SUMMARY

Various system embodiments comprise a lead having a distal end and aproximal end. The distal end includes a plurality of electrodes. Thelead is configured to be fed into a dorsal epidural space of a human toa desired region of a spinal column and to be fed laterally to at leastpartially encircle a spinal cord in the desired region to place at leastone stimulation electrode in position to stimulate a dorsal nerve rootand at least another stimulation electrode in position to stimulate aventral nerve root. The desired region may include cervical vertebrae,thoracic vertebrae, or lumbar vertebrae. Some embodiments stimulate thespinal cord in the T1-T5 region.

Various system embodiments comprise means for vertically feeding a leadthrough a dorsal epidural space proximate to a desired vertebra, andlaterally passing the lead proximate to a dorsal nerve root and aventral nerve root, and means for fixing the lead in position tooperatationally place at least one electrode in position to stimulate atleast one of a dorsal nerve root or a ventral nerve root.

According to various method embodiments for implanting a spinal cordstimulation lead, the lead is introduced into a dorsal epidural space,and fed through the dorsal epidural space proximate to a desiredvertebra. The lead is passed proximate to a dorsal nerve root and aventral nerve root. At least one electrode is positioned operationallyproximate to the dorsal nerve root to capture at least a portion of thedorsal nerve root with electrical stimulation delivered using the atleast one electrode. At least another electrode is positionedoperationally proximate to the ventral nerve root to capture at least aportion of the ventral nerve root with electrical stimulation deliveredusing the at least another electrode.

This Summary is an overview of some of the teachings of the presentapplication and not intended to be an exclusive or exhaustive treatmentof the present subject matter. Further details about the present subjectmatter are found in the detailed description and appended claims. Otheraspects will be apparent to persons skilled in the art upon reading andunderstanding the following detailed description and viewing thedrawings that form a part thereof, each of which are not to be taken ina limiting sense. The scope of the present invention is defined by theappended claims and their equivalents.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1A illustrates a spinal column, including the T1-T5 vertebrae, froma posterior or dorsal perspective, and FIG. 1B illustrates a side viewof the spinal column

FIG. 2 illustrates a perspective view of a portion of the spinal column.

FIG. 3 illustrates a top view of a cross section of the spinal column.

FIG. 4 illustrates an embodiment of a method for implanting a lead foruse in delivering spinal cord stimulation.

FIG. 5 illustrates sympathetic pathways extending from ventral anddorsal nerve roots.

FIG. 6 illustrates a portion of the spinal cord, with nerve rootsextending from three vertebral locations, and further illustrates aneural stimulation lead fed through the dorsal epidural space and atleast partially around the spinal cord to operationally set electrodesin place to stimulate and/or inhibit activity in the dorsal and ventralnerve roots, according to various embodiments.

FIG. 7 illustrates a multi-lead embodiment to stimulate dorsal andventral nerve roots on contralateral sides of the spinal cord.

FIG. 8 illustrates multiple electrodes on a lead wrapped at leastpartially around the spinal cord, where at least some of the electrodesare operationally positioned for use to stimulate the dorsal nerve rootand some of the electrodes are operationally positioned for use tostimulate the ventral nerve root.

FIG. 9 illustrates an embodiment that includes a pre-formed lead madewith a material having a shape memory, where the lead resumes itspreformed shape to at least partially wrap around the spinal cord whenthe lead exits a catheter used to deliver the lead to the stimulationsite.

FIGS. 10A and 10B illustrate a steerable lead embodiment used to placestimulation electrodes in operational position to stimulate ventral anddorsal nerve leads.

FIGS. 11A-11C illustrate an embodiment of a steerable lead.

FIG. 12 illustrates a steerable catheter embodiment used to deliver alead to place stimulation electrodes from the lead in operationalposition to stimulate ventral and dorsal nerve leads.

FIGS. 13A-13C illustrate an embodiment of a steerable catheter.

FIG. 14 illustrates a lead embodiment with a plurality of ringelectrodes.

FIGS. 15A-15B illustrate a lead embodiment with multiple electrodes on acircumference of the lead.

FIGS. 16A-16B illustrate a lead embodiment with multiple electrodes on apaddle-like distal end.

FIG. 17 illustrates a method embodiment to implant the spinal cordstimulation lead to establish and maintain efficacious stimulationtherapy.

FIG. 18 illustrates a system used to deliver spinal cord stimulation,according to various embodiments.

DETAILED DESCRIPTION

The following detailed description of the present subject matter refersto the accompanying drawings which show, by way of illustration,specific aspects and embodiments in which the present subject matter maybe practiced. These embodiments are described in sufficient detail toenable those skilled in the art to practice the present subject matter.Other embodiments may be utilized and structural, logical, andelectrical changes may be made without departing from the scope of thepresent subject matter. References to “an”, “one”, or “various”embodiments in this disclosure are not necessarily to the sameembodiment, and such references contemplate more than one embodiment.The following detailed description is, therefore, not to be taken in alimiting sense, and the scope is defined only by the appended claims,along with the full scope of legal equivalents to which such claims areentitled.

A known spinal cord stimulation system contains a straight lead bodywith multiple electrodes, which only allows for one-dimensional movementalong the spinal cord. The vertical, one-dimensional access within theepidural space limits the ability of the device to selectively stimulateneural pathways, to position the electrodes with respect to the neuraltargets in a desired position to promote a desired efficacy of thestimulation, and to avoid loss of nerve capture due to migration ormovements of the lead in the epidural space. Some issues with this leaddesign include lead migration and the inability to precisely stimulatethe dorsal and ventral nerve root.

Various embodiments that provide neural stimulation treatmentselectively stimulate sympathetic afferent and/or efferent neurones onthe thoracic spinal cord. The system, device and method provide aversatile way to stimulate neural targets in the spinal cord region.Sympathetic modulation (inhibition or activation of sympatheticactivity) treats a variety of cardiovascular disease with abnormalsympathetic activity. The neural stimulation is capable of beingimplemented in treatments for pain, heart failure, arrhythmia, angina,and the like. Various embodiments activate sympathetic afferent (e.g.relatively low frequency dorsal horn stimulation) or activatesympathetic efferent (e.g. relatively low frequency ventral hornstimulation) or inhibit or block sympathetic efferent (e.g. relativelyhigh frequency ventral horn stimulation). Some embodiments test andappropriately modify the therapy delivery by testing the sympatheticresponse (e.g., heart rate and blood pressure changes) and using theelectrodes which are operationally-positioned to stimulate the selectedneurons.

Various embodiments that deliver electrodes for spinal cord stimulationprovide a steerable design, which is capable of selectively stimulatingsympathetic afferent pathways in the dorsal nerve root, sympatheticefferent pathways in the ventral nerve root, or both sympatheticafferent and efferent pathways. The lead can be moved vertically up anddown along the spinal cord. Once the targeted region is reached, such asin the T1-T5 region, the lead body is capable of being steered to bendand curve around the spinal cord. Some embodiments target other regionsof the spinal column, such as various regions in the cervical, thoracicor lumbar areas. Some embodiments cause the lead to contract around atleast a portion of the spinal cord or other structure of the spinalcolumn. The contraction is appropriate to fix the electrodes in positionwith respect to the spinal cord without providing an undesirably highforce against the spine. Various lead embodiments provide multipleelectrodes along both the ventral and dorsal horn of the spinal column,allowing the electric current to be delivered to either activatesympathetic afferent (low frequency dorsal horn stimulation) or activatesympathetic efferent (low frequency ventral horn stimulation) orelectric blocking sympathetic efferent (high frequency ventral hornstimulation). Some embodiments test and appropriately modify the therapydelivery by testing the sympathetic response (e.g., heart rate and bloodpressure changes) and using the electrodes which areoperationally-positioned to stimulate the selected neurons.

Physiology

Provided below is a brief discussion of some diseases capable of beingtreated using the present subject matter and the nervous system. Thisdiscussion is believed to assist a reader in understanding the disclosedsubject matter.

Diseases

The present subject matter can be used to prophylactically ortherapeutically treat various diseases by modulating autonomic tone.Examples of such diseases or conditions include hypertension, cardiacremodeling, and heart failure.

Hypertension is a cause of heart disease and other related cardiacco-morbidities. Hypertension occurs when blood vessels constrict. As aresult, the heart works harder to maintain flow at a higher bloodpressure, which can contribute to heart failure. Hypertension generallyrelates to high blood pressure, such as a transitory or sustainedelevation of systemic arterial blood pressure to a level that is likelyto induce cardiovascular damage or other adverse consequences.Hypertension has been defined as a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mm Hg. Consequences ofuncontrolled hypertension include, but are not limited to, retinalvascular disease and stroke, left ventricular hypertrophy and failure,myocardial infarction, dissecting aneurysm, and renovascular disease. Alarge segment of the general population, as well as a large segment ofpatients implanted with pacemakers or defibrillators, suffer fromhypertension. The long term mortality as well as the quality of life canbe improved for this population if blood pressure and hypertension canbe reduced. Many patients who suffer from hypertension do not respond totreatment, such as treatments related to lifestyle changes andhypertension drugs.

Following myocardial infarction (MI) or other cause of decreased cardiacoutput, a complex remodeling process of the ventricles occurs thatinvolves structural, biochemical, neurohormonal, and electrophysiologicfactors. Ventricular remodeling is triggered by a physiologicalcompensatory mechanism that acts to increase cardiac output due toso-called backward failure which increases the diastolic fillingpressure of the ventricles and thereby increases the so-called preload(i.e., the degree to which the ventricles are stretched by the volume ofblood in the ventricles at the end of diastole). An increase in preloadcauses an increase in stroke volume during systole, a phenomena known asthe Frank-Starling principle. When the ventricles are stretched due tothe increased preload over a period of time, however, the ventriclesbecome dilated. The enlargement of the ventricular volume causesincreased ventricular wall stress at a given systolic pressure. Alongwith the increased pressure-volume work done by the ventricle, this actsas a stimulus for hypertrophy of the ventricular myocardium. Thedisadvantage of dilatation is the extra workload imposed on normal,residual myocardium and the increase in wall tension (Laplace's Law)which represent the stimulus for hypertrophy. If hypertrophy is notadequate to match increased tension, a vicious cycle ensues which causesfurther and progressive dilatation. As the heart begins to dilate,afferent baroreceptor and cardiopulmonary receptor signals are sent tothe vasomotor central nervous system control center, which responds withhormonal secretion and sympathetic discharge. It is the combination ofhemodynamic, sympathetic nervous system and hormonal alterations (suchas presence or absence of angiotensin converting enzyme (ACE) activity)that ultimately account for the deleterious alterations in cellstructure involved in ventricular remodeling. The sustained stressescausing hypertrophy induce apoptosis (i.e., programmed cell death) ofcardiac muscle cells and eventual wall thinning which causes furtherdeterioration in cardiac function. Thus, although ventricular dilationand hypertrophy may at first be compensatory and increase cardiacoutput, the processes ultimately result in both systolic and diastolicdysfunction (decompensation). It has been shown that the extent ofventricular remodeling is positively correlated with increased mortalityin post-MI and heart failure patients.

Heart failure (HF) refers to a clinical syndrome in which cardiacfunction causes a below normal cardiac output that can fall below alevel adequate to meet the metabolic demand of peripheral tissues. Heartfailure may present itself as congestive heart failure (CHF) due to theaccompanying venous and pulmonary congestion. Heart failure can be dueto a variety of etiologies such as ischemic heart disease. Heart failurepatients have reduced autonomic balance, which is associated with LVdysfunction and increased mortality.

Nervous System

The autonomic nervous system (ANS) regulates “involuntary” organs, whilethe contraction of voluntary (skeletal) muscles is controlled by somaticmotor nerves. Examples of involuntary organs include respiratory anddigestive organs, and also include blood vessels and the heart. Often,the ANS functions in an involuntary, reflexive manner to regulateglands, to regulate muscles in the skin, eye, stomach, intestines andbladder, and to regulate cardiac muscle and the muscle around bloodvessels, for example.

The ANS includes the sympathetic nervous system and the parasympatheticnervous system. The sympathetic nervous system is affiliated with stressand the “fight or flight response” to emergencies. Among other effects,the “fight or flight response” increases blood pressure and heart rateto increase skeletal muscle blood flow, and decreases digestion toprovide the energy for “fighting or fleeing.” The parasympatheticnervous system is affiliated with relaxation and the “rest and digestresponse” which, among other effects, decreases blood pressure and heartrate, and increases digestion to conserve energy. The ANS maintainsnormal internal function and works with the somatic nervous system.Afferent nerves convey impulses toward a nerve center, and efferentnerves convey impulses away from a nerve center.

The heart rate and force is increased when the sympathetic nervoussystem is stimulated, and is decreased when the sympathetic nervoussystem is inhibited (the parasympathetic nervous system is stimulated).Cardiac rate, contractility, and excitability are known to be modulatedby centrally mediated reflex pathways. Baroreceptors and chemoreceptorsin the heart, great vessels, and lungs, transmit cardiac activitythrough vagal and sympathetic afferent fibers to the central nervoussystem. Activation of sympathetic afferents triggers reflex sympatheticactivation, parasympathetic inhibition, vasoconstriction, andtachycardia. In contrast, parasympathetic activation results inbradycardia, vasodilation, and inhibition of vasopressin release. Amongmany other factors, decreased parasympathetic or vagal tone or increasedsympathetic tone is associated with various arrhythmias genesis,including ventricular tachycardia and atrial fibrillation.

Stimulating the sympathetic and parasympathetic nervous systems can haveeffects other than heart rate and blood pressure. For example,stimulating the sympathetic nervous system dilates the pupil, reducessaliva and mucus production, relaxes the bronchial muscle, reduces thesuccessive waves of involuntary contraction (peristalsis) of the stomachand the motility of the stomach, increases the conversion of glycogen toglucose by the liver, decreases urine secretion by the kidneys, andrelaxes the wall and closes the sphincter of the bladder. Stimulatingthe parasympathetic nervous system (inhibiting the sympathetic nervoussystem) constricts the pupil, increases saliva and mucus production,contracts the bronchial muscle, increases secretions and motility in thestomach and large intestine, and increases digestion in the smallintention, increases urine secretion, and contracts the wall and relaxesthe sphincter of the bladder. The functions associated with thesympathetic and parasympathetic nervous systems are many and can becomplexly integrated with each other.

Neural stimulation can be used to stimulate nerve traffic or inhibitnerve traffic. An example of neural stimulation to stimulate nervetraffic is a lower frequency signal (e.g. within a range on the order of20 Hz to 50 Hz). An example of neural stimulation to inhibit nervetraffic is a higher frequency signal (e.g. within a range on the orderof 120 Hz to 150 Hz). Other methods for stimulating and inhibiting nervetraffic have been proposed.

Modulation of the autonomic nervous system has potential clinicalbenefit in preventing remodeling and death in heart failure and post-MIpatients. Electrical stimulation can be used to inhibit sympatheticnerve activity and reduce blood pressure by decreasing vascularresistance. Sympathetic inhibition, which increases parasympathetictone, has been associated with reduced arrhythmia vulnerabilityfollowing a myocardial infarction, presumably by increasing collateralperfusion of the acutely ischemic myocardium and decreasing myocardialdamage.

Spinal Cord

FIG. 1A illustrates a spinal column 100, including the T1-T5 vertebrae101, and further illustrates ribs 102 from a posterior or dorsalperspective. FIG. 1B illustrates a side view of the spinal column,including the T1-T5 vertebrae 101 of the column, and the ribs 102. Thesefigures also illustrate a lateral axis, a vertical axis in the cranial(up) or caudal (down) direction, and a posterior or dorsal direction andan anterior or ventral direction.

The spinal column includes cervical, thoracic and lumbar areas.Vertebrae form the building blocks of the spinal column and protect thespinal cord. T1-T5 are the uppermost (cranial) portion of the thoracicarea of the spinal column. Projections from T1-T5 innervate the heart.The spinal projections from T1-T5 are sympathetic. Increased efferentsympathetic activity increases heart rate and contractility. Afferent(e.g. pain signals) for the heart tissue also go throughout spinalsegments T1-T5. Various embodiments target the T1-T5 region forcardiovascular disease applications. Other regions may be targeted forother applications (e.g. treatment for hypertension, diabetes, obesity,etc.).

FIG. 2 illustrates a perspective view of a portion of the spinal column.As illustrated, the vertebrae includes a vertebral body 203 and a bonyring 204 attached to the vertebral body 203. The stacked vertebraeprovide a vertebral canal that protects the spinal cord 205. The spinalcord is nerve tissue that carries neural messages between the brain andparts of the body. Nerve roots branch off and exit the spine on bothsides through spaces between the vertebra. The spinal cord is surroundedby dura matter, which holds spinal fluid that surrounds the spinal cord.The space between the walls and the dura matter of the vertebral canalis referred to as epidural space 206. Some embodiments of the presentsubject matter steer a lead through the dorsal epidural space 206 to theT1-T5 region, and some embodiments steer a catheter through the dorsalepidural space to the T1-T5 region.

FIG. 3 illustrates a top view of a cross section of a vertebra in thespinal column. The vertebra includes a vertebral body 303 and a bonyring 304 that includes the spinous process. The vertebrae provide aspinal canal that contains the spinal cord. The illustrated spinal cordincludes white matter 307 and gray matter 308. Spinal nerves 309A, 309Bextend from the sides of the spinal column. Each spinal nerve 309A, 309Bhas a dorsal nerve root 310A, 310B and a ventral nerve root 311A, 311B.The front or ventral gray column of the spinal cord is referred to asthe ventral horn 312A, 312B, which is a longitudinal subdivision of graymatter in the anterior part of each lateral half of the spinal cord thatcontains neurons giving rise to motor fibers of the ventral roots of thespinal nerves. The posterior gray column of the spinal cord is referredto as the dorsal horn 313A, 313B, which is a longitudinal subdivision ofgray matter in the dorsal part of each lateral half to the spinal cordthat receives terminals from some afferent fibers of the dorsal roots ofthe spinal nerves. The ventral root 311A, 311B is the efferent motorroot of a spinal nerve. The dorsal root 310A, 310B is the afferentsensory root of the spinal nerve. The ventral root joins with the dorsalroot to form a mixed spinal nerve 309A, 309B. The distal end of thedorsal root includes the dorsal root ganglion which contains the neuroncell bodies of the nerve fibers conveyed by the root.

The afferent sympathetic pathway includes neuron bodies in the dorsalroot ganglia, and neuron bodies in the dorsal horn. The efferentsympathetic pathway includes preganglionic motor neuron bodies in theintermediolateral column of the spinal cord from to T4/T5, andpostganglionic motor neuron bodies in superior, middle and inferiorcervical ganglias and in cell T1 thoracic ganglias from T1 to T4/T5.Various embodiments modulate sympathetic efferent and afferent activityby delivering electric current to selected regions of the thoracicspinal cord. Some embodiments provide a three-dimensional, steerablelead design. The lead can be moved up and down along the spinal column.At the targeted region, the lead body is capable of being steered tobend and curve around the spinal cord. This lead placement providesmultiple electrodes located along both the ventral and dorsal horn ofthe spinal cord. Selected electrodes are used to selectively modulateafferent, efferent or both afferent and efferent pathways. Thus, adesired therapy is provided by choosing electrodes that are closest tosympathetic neurons.

FIG. 4 illustrates sympathetic pathways extending from ventral anddorsal nerve roots. The gray matter of the spinal cord 405 includesventral horns 412A, 412B and dorsal horns 413A, 413B. The ventral root411 is the efferent motor root of a spinal nerve. The dorsal root 412 isthe afferent sensory root of the spinal nerve. The ventral root joinswith the dorsal root to form a mixed spinal nerve.

FIG. 5 illustrates an embodiment of a method for implanting a lead foruse in delivering spinal cord stimulation. The patient can sit or lie ontheir side in a position of back flexion to open the intervertebralspaces. Depending on the implant location, the appropriate lumbar spaceis identified using Tuffier's line as a reference point. Using a steriletechnique the spinal lead introducer is inserted in the midline, whileaiming cranially. As the needle is pushed forward, there is resistanceas it passes through the ligamentum flavae. The loss of resistance isevidence that the epidural space has been penetrated. Once in theepidural space 506, the lead can be deployed through the introducer andthen passed into the epidural space, and then up to the T1-T5 region andaround at least a portion of the spinal cord 505.

FIG. 6 illustrates a portion of the spinal cord 605, with nerve rootsextending from three vertebral locations, and further illustrates aneural stimulation lead 614 fed through the dorsal epidural space(behind the illustrated cord 605) and least partially around the spinalcord to operationally set electrodes in place to stimulate and/orinhibit activity in the dorsal and ventral nerve roots 611, 612,according to various embodiments. The pulse generator 615 can beimplanted in an appropriate location, such as in an abdominal region orin or just above the buttocks. During the implantation procedure, theproximate end of the lead can be connected to an external device used togenerate stimulation pulses and monitor the efficacy of the leadplacement.

FIG. 7 illustrates a multi-lead embodiment to stimulate dorsal andventral nerve roots on contralateral sides of the spinal cord. Theillustrated figure shows two leads exiting from a pulse generator 715.One lead 714A is directed around a first side, and a second lead 714B isdirected around a second side. Electrodes on each lead are placedoperationally in position with respect to the nerve root(s) to stimulatethe neural target(s) and elicit the desired effect(s).

FIG. 8 illustrates multiple electrodes on a lead 814 wrapped at leastpartially around the spinal cord 805, where at least some of theelectrodes 816A are operationally positioned for use to stimulate thedorsal nerve root 812 and some of the electrodes 816B are operationallypositioned for use to stimulate the ventral nerve root 811. Each leadincludes a plurality of electrodes that are adapted to be combined togenerate various stimulation vectors. Thus, an appropriate combinationof electrodes can be used to generate a stimulation field thateffectively stimulates the desired neural target(s), and in someembodiments, avoid possible undesired effects of neural stimulation.

Some benefits of the present subject matter include more therapychoices, including efferent, afferent, and both efferent and afferenttargets. Some embodiments provide simultaneous afferent and efferentmodulation. For example, chronic intermittent sympathetic efferentstimulation could be used to alter the progression of HF. Meanwhile, asensed tachy event could trigger sympathetic afferent stimulation toinhibit the occurrence of a ventricular arrhythmia. Some embodimentsprovide the capability of altering afferent and efferent modulation toprovide a more robust therapy. For example, in HF patients, chronicsympathetic afferent stimulation and chronic sympathetic efferent blockor inhibition could be applied in an alternating order to inhibitsympathetic activity, while also preventing desensitization. Someembodiments provide the ability to monitor and adjust the stimulation toprovide and/or maintain a desired efficacy (capture neural target and/oravoid or abate side effects) of the therapy. Some lead embodimentspromote stable lead placement, which prevents or abates lead migrationand movement.

Some embodiments of the present subject matter provide a treatment fortachyarrhythmia. For example, some embodiments deliver sympatheticafferent stimulation at the dorsal horn of the spinal cord with arelatively low frequency to reflexively inhibit sympathetic activity;and some embodiments deliver direct sympathetic efferent inhibition witha relatively high frequency stimulation at the ventral horn of thespinal column. Some embodiments of the present subject matter provide atreatment for heart failure. For example, some embodiments enhancesympathetic activity periodically with chronic intermittent efferentstimulation at the ventral horn of the spinal column with a relativelylow frequency. Some embodiments inhibit or block sympathetic efferentactivity, either chronically or intermittently, using a high frequencyelectrical stimulation at the ventral horn of the spinal cord.

Lead/Catheters

An embodiment uses a steerable delivery catheter (e.g. using stereotaxismagnetic guidance) or other guidance means to aid in positioning thelead in the targeted region of the epidural space. Some catheterembodiments are steerable in two axes (vertical, also referred to ascranial/caudal axis, and lateral axis). Some lead embodiments have adistal “J” biased tip designed to wrap around the spinal cord when thelead is deployed from the delivery catheter to the targeted region. TheJ-biased tip aids in retaining the electrodes in place, avoiding orabating lead migration. Additionally, the J-biased tip maintains contactwith the spinal column, keeping the stimulation electrodes desirablyclose to the ventral and/or dorsal nerve roots. The delivery catheter isthen peeled or cut away from the lead, leaving the lead in position.

An embodiment uses a steerable stimulation lead to aid in positioningthe lead in the targeted region of the epidural space. Some leadembodiments are steerable in two axes (vertical or cranial/caudal axis,and lateral axis). Some lead embodiments are adapted to be locked orfixed in a fixed position, aiding in retaining the electrodes in placeand maintaining contact with the spinal column, keeping the stimulationelectrodes desirably close to the ventral and/or dorsal nerve roots. Forexample, some embodiments use a chuck to hold the lead in position.Other designs can be used to fix or stabilize the position of the lead.A position fixation apparatus on a proximal end of the lead can be usedto maintain a shape and position of a distal end of the lead.

FIG. 9 illustrates an embodiment that includes a pre-formed lead madewith a material having a shape memory, where the lead 914 resumes itspreformed shape to at least partially wrap around the spinal cord 905(or potentially some other structures of the spinal column) when thelead exits a catheter 917 used to deliver the lead to the stimulationsite. The illustrated portion of the pre-formed lead has a plurality ofelectrodes 916, various combinations of which can be selected togenerate a desired neural stimulation field to stimulate a desiredneural target. The lead is designed with appropriate materialcharacteristics to provide an appropriate force when contracting backinto its preformed shape. In some embodiments, the force of contractionis sufficient to fix the lead in position or to discourage leadmigration.

FIGS. 10A and 10B illustrate a steerable lead embodiment used to placestimulation electrodes in operational position to stimulate ventral anddorsal nerves, the illustrated lead 1014 includes a plurality ofelectrodes 1016. As is illustrated in an embodiment below, the lead isdesigned to be steered in at least two directions, to allow the lead tobe steered from the dorsal epidural space around at least a portion ofspinal cord 1005 to stimulate the nerve root(s). A steering tendon orguy wire can be used to contract the lead around the spinal cord,fixating the electrodes in operational position to stimulate the ventraland/or dorsal nerve roots.

FIGS. 11A-11C illustrate an embodiment of a steerable lead. The leadbody 1114 includes a distal end 1116. A lumen adapted to receive asteering tendon 1118 is in the lead body 1114. The lead body 1114includes a compressible or expandable side 1119 and a noncompressible orexpandable side 1120. The steering tendon is appropriately connected tothe compressible or expandable side to control the compression orexpansion of that side. When the lead is implanted, the lead is steeredby appropriately controlling the tendon.

FIG. 12 illustrates a steerable catheter embodiment used to deliver alead to place stimulation electrodes from the lead in operationalposition to stimulate ventral and dorsal nerve leads. A first steeringtendon 1221 is attached to a first anchor member 1222 located at adistal portion of the pre-formed distal end 1223. A second steeringtendon 1224 is attached to a second anchor member 1225 located distal tothe deflection area 1226.

The anchor members 1222, 1225 can be constructed using various materialsand construction methods known in the art, including simply bonding adistal part of the tendon to the shaft. In the illustratedconfiguration, the anchor members 404, 408 are formed of stainless steelrings to which steering tendons can be welded or soldered. The steeringtendons may be attached to the anchor members using a mechanicalinterference fit such as a crimp or a stop member. The steering tendonsare typically made of metallic (e.g. stainless steel) members such assolid wire, braided wire, or ribbon material. It is possible to formtendons from non-metallic members such as high strength compositemembers (e.g. Kevlar, carbon fiber).

Some embodiments embed the anchor members within the walls of the leadshaft 1214 during shaft construction. In some embodiments, the anchormembers are adhered to the inner wall of the lead shaft 1214 by adhesivebonding or hot melting the shaft material. Hot melting may be performedby heating the anchor members while in intimate contact with the innerwalls of the shaft. Another method of attaching the anchor membersinvolves butting the bands against a support structure of the shaft 102such as a reinforcement cage or braid.

FIGS. 13A-13C illustrate an embodiment of a steerable catheter. FIG. 13Ais an external view of the catheter including a proximal handle assembly1328. The proximal handle assembly 1328 typically includes a grip 1329and a steering member 1330. The handle assembly 1328 can be constructedby principles known in the art, such as described in U.S. Pat. Nos.6,096,036 and 6,270,496, which are hereby incorporated by reference intheir respective entireties.

FIG. 13B is a cross section of a distal part of the catheter shaftroughly corresponding to section B-B in FIG. 13A. A shaft embodiment1331 includes a wall 1332 formed of polymer, typically a high durometerPebax material. The shaft wall encloses a stylet 1333, typically made ofa resilient, shape-memory member such as a wire formed of nitinol wireor other superelastic alloy. A nitinol stylet is preshaped by heatingthe stylet while it is being constrained in the desired shape. A styletformed in this way is then inserted into the shaft to impart thepreformed shape at the distal end 1334 of the shaft 1331. The stylet istypically affixed at or near the tip of the shaft to prevent migrationof the stylet within the catheter during use.

In the illustrated figures, the wall of the shaft also enclosesconductors 1335 coupled to the electrodes. Also shown within the shaftare the steering tendons 1336, 1337. The steering tendons are disposedwithin lumens, which are typically formed of a lubricous material suchas PTFE and may be affixed to an inner surface of the shaft wall.

FIG. 13C shows a cross section of a proximal part of the catheter shaft1331. The layout of the shaft is similar to that seen in FIG. 13B, andadditionally shows a reinforcing member 1338 and an outer casing 1339.The reinforcing member can include a braid, cage, ribbon, or otherreinforcing member that provides axial and torsional stiffness to theshaft while still allowing a reasonable amount of bending in the shaft.The outer casing may be made of a Pebax material having a similardurometer as the shaft wall, or may be made of a different materialhaving unique protective and/or lubricous properties. The differencesbetween the distal and proximal cross sections (e.g. inclusion of aproximal support member) as seen in FIGS. 13B and 13C result in theproximal portion having greater stiffness than the distal portion. Othervariations in stiffness may also be advantageously induced alongportions of the flexible shaft. To vary stiffness of the shaft, thebending properties of the shaft wall may be changed (e.g. the durometerof the polymeric materials) or the stylet characteristics (e.g. outerdiameter or cross section) can be varied along the shaft length. Varyingthe stiffness along the length of the shaft can beneficially enhance thedeflectability of the steered sections or to tune the stiffness of thedistal end to minimize the risk of trauma.

A number of electrode configurations can be used. The illustrationsincluded herein are provided as examples, and are not intended to be anexhaustive listing of possible configurations.

FIG. 14 illustrates a lead embodiment with a plurality of ringelectrodes. The figure illustrates an embodiment of a lead 1414 withannular stimulation electrodes 1416 that form an electrode region, suchas used to selectively stimulate the ventral nerve root or dorsal nerveroot, according to various embodiments. Any one or combination of theannular stimulation electrodes can be used to deliver the neuralstimulation to the desired neural target.

FIGS. 15A-15B illustrate a lead embodiment with multiple electrodes on acircumference of the lead. The illustrated electrodes 1516 do notcircumscribe the lead 1514. Thus, a subset of the illustrated electrodescan be selected to provide directional stimulation. For example, thelead may twist or rotate as it is fed into position, and it may bedesired to stimulate a neural target on one side of the lead withoutstimulating other nerves or tissue on the other sides of the lead. Forexample, root nerves extending from one vertebrae can be stimulatedwithout stimulating root nerves extending from other vertebrae. A neuralstimulation test routine can cycle through the available electrodes foruse in delivering the neural stimulation to determine which subset ofelectrodes are facing toward the neural target. FIG. 15B illustrates anexample with four electrodes separated around the lead, approximately 90degrees apart. Other electrode arrangements and spacing can be used,such as, by way of example and not limitation, 2 electrodes spacedaround the circumference approximately 45 degrees apart, approximately90 degrees apart or approximately 180 degrees apart; or 3 electrodesspaced around the circumference approximately 120 degrees, approximately60 degrees or approximately 30 degrees apart.

FIGS. 16A-16B illustrate a lead embodiment with multiple electrodes on apaddle-like distal end. The paddle-like distal end 1640 has a relativelyflat profile. The electrodes 1616 are positioned on one side of thepaddle, such that the electric stimulation field is generated on oneside of the paddle-like distal end.

FIG. 17 illustrates a method embodiment to implant the spinal cordstimulation lead to establish and maintain efficacious stimulationtherapy. At 1741, a lead is inserted into an epidural space. Exampleswere discussed with respect to FIG. 5 and with respect to varioussteerable lead and steerable catheter designs. At 1742, the lead (orcatheter) is steered to direct the lead laterally adjacent to and atleast partially around the spinal cord to position the electrodes on thelead operationally proximate to the dorsal and/or ventral nerve roots ina location in the T1-T5 range. At 1743, the electrode positions aretested to determine if the electrode positions provide efficaciousstimulation. For example, some embodiments monitor one or morephysiological parameters to verify capture of the neural target (e.g.ventral and/or dorsal nerve roots). The present subject matter iscapable of selectively stimulating or targeting only the ventral nerveroot and/or selectively stimulating the dorsal nerve root. Someembodiments monitor one or more physiological parameter to abatepotential unintended responses to the neural stimulation. If unable toverify capture or if undesired side effects are present during theimplantation process, the process adjusts the physical positioningand/or the electronic positioning in an effort to realize efficaciousstimulation, as represented at 1744. The physical repositioning involvesphysically moving (e.g. pushing, pulling, rotating, contracting aroundspinal cord) the lead. The electronic repositioning involves selectingvarious combinations of electrodes to adjust the direction and positionof the electric stimulation field. Electronic repositioning can beperformed as part of an automatic process, where a device cycles throughavailable electrode combinations (and stimulation intensity) until thedesired efficacy is realized. Electronic repositioning can be controlledby a technician during the implant procedure. Some embodiments use acombination of technician control of potential configurations, and anautomatic test routine.

When efficacious stimulation is detected, the physical lead placement isset at 1745. A proximal end of the lead is connected to an implantablepulse generator, which may be, for example, implanted in the small ofthe back. At 1746, therapy is delivered using the implanted lead and theimplanted pulse generator. At 1747, the implanted pulse generatorintermittently tests for efficacious stimulation to verify captureand/or abate side effects of the stimulation. If appropriate, theelectronic positioning is adjusted to deliver efficacious stimulation,as illustrated at 1748. This electronic repositioning can be performedautomatically, controlled by a technician using a programmer, or acombination thereof.

FIG. 18 illustrates a system used to deliver spinal cord stimulation,according to various embodiments. The illustrated neural stimulatorembodiment 1850 includes a neural stimulation circuit 1851, a feedbackcircuit 1852, a controller 1853, and memory 1854. The illustratedembodiment further includes at least one port 1855 to connect to atleast one lead 1856. At least one lead is adapted to be fed into thedorsal epidural space to the T1-T5 region, and directed at leastpartially around the spinal cord to stimulate the ventral and/or dorsalnerve root. The neural stimulation circuit is connected to the port(s)to provide a neural stimulation signal to at least one neuralstimulation electrode 1857 on the lead(s) to elicit a desired neuralresponse when an appropriate signal is provided to anappropriately-positioned neural stimulation electrode. The feedbackcircuit is connected to the port(s) to receive a signal from thephysiology sensor 1858. The physiology sensor may be on a different leadthan the lead fed into the epidural space to stimulate the nerveroot(s). Some embodiments receive a feedback signal from otherimplantable medical devices, such as a pacemaker or anti-arrhythmiadevice. The sensor senses a physiology function that depends, at leastin part, on the neural stimulation. Examples of such functions includesheart rate, blood pressure, ECG waveforms, respiration, andacceleration/motion. Thus, various embodiments implement a heart ratesensor as the physiology sensor, and various embodiments implement ablood pressure sensor as the physiology sensor. One example of such asensor is an acoustic sensor adapted to sense blood flow. The sensedblood flow is capable of being used to determine blood pressure and/orheart rate. However, other sensor technology can be used.

The illustrated system includes a communication module 1859 adapted tocommunicate with other devices. For example, some embodimentscommunicate using telemetry. Various embodiments wirelessly communicatefrom the implanted device to external devices, such as a programmer1860. Various embodiments communicate, either through a wired connectionor a wireless connection, to other implantable medical devices 1861.Example of other implantable medical devices include cardiac rhythmmanagement devices, such as a pacemaker, cardiodefibrillator, and thelike, and further include implantable neural stimulators. According tosome embodiments, such other implantable medical devices sensephysiological parameters that are affected by the stimulation of thenerve root, and communicate information regarding the sensedphysiological parameters during an implant procedure or while thedevices are chronically implanted in a patient. According to someembodiments, the communication module is adapted to communicate with aportable external device 1862, such as a personal data assistant, atelephone, an interrogator, a laptop computer. According to someembodiments, the portable external device 1862 and programmer 1860 areadapted to communicate over a communication network 1863.

Heart rate and/or blood pressure can be used to determine whether thestimulation is affecting the autonomic system. Additionally, variousautonomic balance indicators (ABIs) can be used to provide feedbackconcerning the neural stimulation therapy directed toward the nerveroot(s). Various embodiments assess ABI using one or variouscombinations of parameters, such as heart rate variability (HRV), heartrate turbulence (HRT), electrogram features, activity, respiration andactivity. These parameters are briefly discussed below. Variousembodiments provide closed loop control of the treatment using ABI.

HRV is one technique that has been proposed to assess autonomic balance.HRV relates to the regulation of the sinoatrial node, the naturalpacemaker of the heart by the sympathetic and parasympathetic branchesof the autonomic nervous system. An HRV assessment is based on theassumption that the beat-to-beat fluctuations in the rhythm of the heartprovide us with an indirect measure of heart health, as defined by thedegree of balance in sympathetic and vagus nerve activity.

The time interval between intrinsic ventricular heart contractionschanges in response to the body's metabolic need for a change in heartrate and the amount of blood pumped through the circulatory system. Forexample, during a period of exercise or other activity, a person=sintrinsic heart rate will generally increase over a time period ofseveral or many heartbeats. However, even on a beat-to-beat basis, thatis, from one heart beat to the next, and without exercise, the timeinterval between intrinsic heart contractions varies in a normal person.These beat-to-beat variations in intrinsic heart rate are the result ofproper regulation by the autonomic nervous system of blood pressure andcardiac output; the absence of such variations indicates a possibledeficiency in the regulation being provided by the autonomic nervoussystem. One method for analyzing HRV involves detecting intrinsicventricular contractions, and recording the time intervals between thesecontractions, referred to as the R-R intervals, after filtering out anyectopic contractions (ventricular contractions that are not the resultof a normal sinus rhythm). This signal of R-R intervals is typicallytransformed into the frequency-domain, such as by using fast Fouriertransform (FFT) techniques, so that its spectral frequency componentscan be analyzed and divided into low and high frequency bands. Forexample, the low frequency (LF) band can correspond to a frequency (f)range 0.04 Hz<f<0.15 Hz, and the high frequency (HF) band can correspondto a frequency range 0.15 Hz<f<0.40 Hz. The HF band of the R-R intervalsignal is influenced only by the parasympathetic/vagal component of theautonomic nervous system. The LF band of the R-R interval signal isinfluenced by both the sympathetic and parasympathetic components of theautonomic nervous system. Consequently, the ratio LF/HF is regarded as agood indication of the autonomic balance between sympathetic andparasympathetic/vagal components of the autonomic nervous system. Anincrease in the LF/HF ratio indicates an increased predominance of thesympathetic component, and a decrease in the LF/HF ratio indicates anincreased predominance of the parasympathetic component. For aparticular heart rate, the LF/HF ratio is regarded as an indication ofpatient wellness, with a lower LF/HF ratio indicating a more positivestate of cardiovascular health. A spectral analysis of the frequencycomponents of the R-R interval signal can be performed using a FFT (orother parametric transformation, such as autoregression) technique fromthe time domain into the frequency domain. Such calculations requiresignificant amounts of data storage and processing capabilities.Additionally, such transformation calculations increase powerconsumption, and shorten the time during which the implantedbattery-powered device can be used before its replacement is required.

One example of an HRV parameter is SDANN (standard deviation of averagedNN intervals), which represents the standard deviation of the means ofall the successive 5 minutes segments contained in a whole recording.Other HRV parameters can be used.

HRT is the physiological response of the sinus node to a prematureventricular contraction (PVC), consisting of a short initial heart rateacceleration followed by a heart rate deceleration. HRT has been shownto be an index of autonomic function, closely correlated to HRV. HRT isbelieved to be an autonomic baroreflex. The PVC causes a briefdisturbance of the arterial blood pressure (low amplitude of thepremature beat, high amplitude of the ensuing normal beat). Thisfleeting change is registered immediately with an instantaneous responsein the form of HRT if the autonomic system is healthy, but is eitherweakened or missing if the autonomic system is impaired.

By way of example and not limitation, it has been proposed to quantifyHRT using Turbulence Onset (TO) and Turbulence Slope (TS). TO refers tothe difference between the heart rate immediately before and after aPVC, and can be expressed as a percentage. For example, if two beats areevaluated before and after the PVC, TO can be expressed as:

${T\; O\mspace{14mu} \%} = {\frac{( {{RR}_{+ 1} + {RR}_{+ 2}} ) - ( {{RR}_{- 2} + {RR}_{- 1}} )}{( {{RR}_{- 2} + {RR}_{- 1}} )}*100.}$

RR⁻² and RR⁻¹ are the first two normal intervals preceding the PVC andRR₊₁ and RR₊₂ are the first two normal intervals following the PVC. Invarious embodiments, TO is determined for each individual PVC, and thenthe average value of all individual measurements is determined. However,TO does not have to be averaged over many measurements, but can be basedon one PVC event. Positive TO values indicate deceleration of the sinusrhythm, and negative values indicate acceleration of the sinus rhythm.The number of R-R intervals analyzed before and after the PVC can beadjusted according to a desired application. TS, for example, can becalculated as the steepest slope of linear regression for each sequenceof five R-R intervals. In various embodiments, the TS calculations arebased on the averaged tachogram and expressed in milliseconds per RRinterval. However, TS can be determined without averaging. The number ofR-R intervals in a sequence used to determine a linear regression in theTS calculation also can be adjusted according to a desired application.

Rules or criteria can be provided for use to select PVCs and for use inselecting valid RR intervals before and after the PVCs. A PVC event canbe defined by an R-R interval in some interval range that is shorterthan a previous interval by some time or percentage, or it can bedefined by an R-R interval without an intervening P-wave (atrial event)if the atrial events are measured. Various embodiments select PVCs onlyif the contraction occurs at a certain range from the precedingcontraction and if the contraction occurs within a certain range from asubsequent contraction. For example, various embodiments limit the HRTcalculations to PVCs with a minimum prematurity of 20% and apost-extrasystole interval which is at least 20% longer than the normalinterval. Additionally, pre-PVC R-R and post-PVC R-R intervals areconsidered to be valid if they satisfy the condition that none of thebeats are PVCs. One HRT process, for example, excludes RR intervals thatare less than a first time duration, that are longer than a second timeduration, that differ from a preceding interval by more than a thirdtime duration, or that differ from a reference interval by apredetermined amount time duration or percentage. In an embodiment ofsuch an HRT process with specific values, RR intervals are excluded ifthey are less than 300 ms, are more than 2000 ms, differ from apreceding interval by more than 200 ms, or differ by more than 20% fromthe mean of the last five sinus intervals. Various embodiments of thepresent subject matter provide programmable parameters, such as any ofthe parameters identified above, for use in selecting PVCs and for usein selecting valid RR intervals before and after the PVCs.

Benefits of using HRT to monitor autonomic balance include the abilityto measure autonomic balance at a single moment in time. Additionally,unlike the measurement of HRV, HRT assessment can be performed inpatients with frequent atrial pacing. Further, HRT analysis provides fora simple, non-processor-intensive measurement of autonomic balance.Thus, data processing, data storage, and data flow are relatively small,resulting in a device with less cost and less power consumption. Also,HRT assessment is faster than HRV, requiring much less R-R data. HRTallows assessment over short recording periods similar in duration totypical neural stimulation burst durations, such as on the order of tensof seconds, for example.

Various embodiments extract various ECG features to provide an ABI.Examples of such features include heart rate, which can be used to formHRV, and HRT. Other features can be extracted from the ECG, and one orvarious combinations of these features can be used to provide an ABI.Various embodiments provide blood pressure to provide an ABI. Forexample, some embodiments sense pulmonary artery blood pressure.

Activity sensors can be used to assess the activity of the patient.Sympathetic activity naturally increases in an active patient, anddecreases in an inactive patient. Thus, activity sensors can provide acontextual measurement for use in determining the autonomic balance ofthe patient. Various embodiments, for example, provide a combination ofsensors to trend heart rate and/or respiration rate to provide anindicator of activity.

Two methods for detecting respiration involve measuring a transthoracicimpedance and minute ventilation. Respiration can be an indicator ofactivity, and can provide an explanation of increased sympathetic tone.For example, it may not be appropriate to change or modify a treatmentfor modulating autonomic tone due to a detected increase in sympatheticactivity attributable to exercise.

Respiration measurements (e.g. transthoracic impedance) can also be usedto measure Respiratory Sinus Arrhythmia (RSA). RSA is the natural cycleof arrhythmia that occurs through the influence of breathing on the flowof sympathetic and vagus impulses to the sinoatrial node. The rhythm ofthe heart is primarily under the control of the vagus nerve, whichinhibits heart rate and the force of contraction. The vagus nerveactivity is impeded and heart rate begins to increase when a breath isinhaled. When exhaled, vagus nerve activity increases and the heart ratebegins to decrease. The degree of fluctuation in heart rate is alsocontrolled significantly by regular impulses from the baroreceptors(pressure sensors) in the aorta and carotid arteries. Thus, ameasurement of autonomic balance can be provided by correlating heartrate to the respiration cycle.

The memory 1854 includes computer-readable instructions that are capableof being operated on by the controller to perform functions of thedevice. Thus, in various embodiments, the controller is adapted tooperate on the instructions to provide programmed neural stimulationtherapies 1864 according to a neural stimulation therapy schedule storedin the memory. Various “closed loop” systems vary the intensity of theneural stimulation, as generally illustrated by the stimulationintensity module 1865, based on the sensed physiology signal received bythe feedback circuit according to a preprogrammed therapy to provide adesired affect. Thus, the closed loop system is capable of reducing andincreasing the neural stimulation intensity as appropriate tomaintaining some measured physiological parameters within an upper andlower boundary during the neural stimulation therapy. Various “openloop” systems without feedback from the physiology signal also can beprogrammed to vary the stimulation intensity. For example, intensity canbe modulated based on a programmed schedule. Various embodimentsmodulate the stimulation intensity by modulating the amplitude of theneural stimulation signal, the frequency of the neural stimulationsignal, the duty cycle of the neural stimulation signal, the duration ofa stimulation signal, the waveform of the neural stimulation signal, thepolarity of the neural stimulation signal, or any combination thereof.

Various embodiments automatically change the electrode configuration, asgenerally illustrated by the electrode configuration module 1866 of thecontroller 1853. The illustrated electrode configuration module isadapted to control switches 1867 to control which electrodes of theavailable electrodes are used to deliver the neural stimulation, and thestimulation vectors for the electrodes. Additionally, the illustratedelectrode configuration module is adapted to work with the stimulationintensity module to control the stimulation intensity for the differentelectrode combinations and stimulation vectors. Thus, for example, theelectrode configuration module can find a reference neural stimulationlevel for a particular electrode combination and vector, and thestimulation intensity module can further modulate the neural stimulationbased on the reference neural stimulation level. A neural stimulationtest routine stored in the memory controls the process of testing for aefficacious electrode configuration from the available electrodeconfigurations.

In various embodiments, the controller automatically implements theneural stimulation test routine, such as in a chronically-implanteddevice. In various embodiments, the controller and a user interfacecooperate to implement a neural stimulation test routine to allow a userto select the at least one of the neural stimulation electrodes to usein delivering the autonomic neural stimulation therapy, such as maybeused in a device to implant the lead into the desired position tostimulate the desired nerve root(s). For example, during an implantationprocedure, the user interface can display test results for variouselectrode configurations. The information identifying the electrodeconfigurations can include the electrodes used in the stimulation, thestimulation amplitude, the stimulation frequency, the stimulation dutycycle, the stimulation duration, the stimulation waveform, and thestimulation polarity. The test results can include the detectedphysiologic response (e.g. heart rate) attributed to the neuralstimulation for an electrode configuration. The user can review the testresults, and select an electrode configuration using the test results.

The illustrated controller includes an event detector 1868, such as maybe used to detect an arrhythmic event or an ischemic event. Upon thedetection of an event, the device appropriately adjusts the therapy forthe event. According to some embodiments, another IMD 1861 detects theevent and communicates the event to the device to adjust the stimulationof the ventral and/or dorsal nerve roots.

Neural Stimulation Therapies

Examples of neural stimulation therapies include neural stimulationtherapies for blood pressure control such as to treat hypertension, forcardiac rhythm management, for myocardial infarction and ischemia, forheart failure, and for pain control. A therapy embodiment involvespreventing and/or treating ventricular remodeling. Activity of theautonomic nervous system is at least partly responsible for theventricular remodeling which occurs as a consequence of an MI or due toheart failure. It has been demonstrated that remodeling can be affectedby pharmacological intervention with the use of, for example, ACEinhibitors and beta-blockers. Pharmacological treatment carries with itthe risk of side effects, however, and it is also difficult to modulatethe effects of drugs in a precise manner. Embodiments of the presentsubject matter employ electrostimulatory means to modulate autonomicactivity, referred to as anti-remodeling therapy or ART. When deliveredin conjunction with ventricular resynchronization pacing, also referredto as remodeling control therapy (RCT), such modulation of autonomicactivity may act synergistically to reverse or prevent cardiacremodeling.

One neural stimulation therapy embodiment involves treating hypertensionby increasing parasympathetic tone (e.g. inhibiting sympatheticactivity) for sustained periods of time sufficient to reducehypertension. Neural stimulation (e.g. sympathetic nerve stimulationand/or parasympathetic nerve inhibition) can mimic the effects ofphysical conditioning. It is generally accepted that physical activityand fitness improve health and reduce mortality. Studies have indicatedthat aerobic training improves cardiac autonomic regulation, reducesheart rate and is associated with increased cardiac vagal outflow. Abaseline measurement of higher parasympathetic activity is associatedwith improved aerobic fitness. Exercise training intermittently stressesthe system and increases the sympathetic activity during the stress.However, when an exercise session ends and the stress is removed, thebody rebounds in a manner that increases baseline parasympatheticactivity and reduces baseline sympathetic activity. Conditioning can beconsidered to be a repetitive, high-level exercise that occursintermittently over time. A conditioning therapy that providesintermittent stress can be applied as therapy for heart failure.

Neural targets in the spinal column can be targeted as part of a therapyfor pain control. The pain control therapy can be used to addresssomatic pain, visceral pain or neuropathic pain. The pain controltherapy can also be used to address acute or chronic pain. According tovarious embodiments, pain control therapies are integrated with othertherapies (e.g. heart failure). Some embodiments provide means for apatient to activate the pain control therapy. This means may use awireless communication from an external device to the implantable pulsegenerator, or a magnetic field such as from a magnet positioned over theimplantable pulse generator. By way of example, a patient who isexperiencing an episode of angina pain may choose to initiate a paincontrol therapy. A physician can program limits on the requested paincontrol therapy, so as to limit the number of times the therapy can berequested over a period of time. Various embodiments implement the paincontrol therapy in conjunction with another therapy to avoid or minimizepain with the therapy. For example, if a defibrillation shock is goingto be applied to a patient, various embodiment implement pain controltherapy in anticipation of delivering the shock.

Myocardial Stimulation Therapies

Various neural stimulation therapies can be integrated with variousmyocardial stimulation therapies. The integration of therapies may havea synergistic effect. Therapies can be synchronized with each other, andsensed data can be shared. A myocardial stimulation therapy provides acardiac therapy using electrical stimulation of the myocardium. Someexamples of myocardial stimulation therapies are provided below.

A pacemaker is a device which paces the heart with timed pacing pulses,most commonly for the treatment of bradycardia where the ventricularrate is too slow. If functioning properly, the pacemaker makes up forthe heart's inability to pace itself at an appropriate rhythm in orderto meet metabolic demand by enforcing a minimum heart rate. Implantabledevices have also been developed that affect the manner and degree towhich the heart chambers contract during a cardiac cycle in order topromote the efficient pumping of blood. The heart pumps more effectivelywhen the chambers contract in a coordinated manner, a result normallyprovided by the specialized conduction pathways in both the atria andthe ventricles that enable the rapid conduction of excitation (i.e.,depolarization) throughout the myocardium. These pathways conductexcitatory impulses from the sino-atrial node to the atrial myocardium,to the atrio-ventricular node, and thence to the ventricular myocardiumto result in a coordinated contraction of both atria and bothventricles. This both synchronizes the contractions of the muscle fibersof each chamber and synchronizes the contraction of each atrium orventricle with the contralateral atrium or ventricle. Without thesynchronization afforded by the normally functioning specializedconduction pathways, the heart's pumping efficiency is greatlydiminished. Pathology of these conduction pathways and otherinter-ventricular or intra-ventricular conduction deficits can be acausative factor in heart failure, which refers to a clinical syndromein which an abnormality of cardiac function causes cardiac output tofall below a level adequate to meet the metabolic demand of peripheraltissues. In order to treat these problems, implantable cardiac deviceshave been developed that provide appropriately timed electricalstimulation to one or more heart chambers in an attempt to improve thecoordination of atrial and/or ventricular contractions, termed cardiacresynchronization therapy (CRT). Ventricular resynchronization is usefulin treating heart failure because, although not directly inotropic,resynchronization can result in a more coordinated contraction of theventricles with improved pumping efficiency and increased cardiacoutput. Currently, a common form of CRT applies stimulation pulses toboth ventricles, either simultaneously or separated by a specifiedbiventricular offset interval, and after a specified atrio-ventriculardelay interval with respect to the detection of an intrinsic atrialcontraction or delivery of an atrial pace.

CRT can be beneficial in reducing the deleterious ventricular remodelingwhich can occur in post-MI and heart failure patients. Presumably, thisoccurs as a result of changes in the distribution of wall stressexperienced by the ventricles during the cardiac pumping cycle when CRTis applied. The degree to which a heart muscle fiber is stretched beforeit contracts is termed the preload, and the maximum tension and velocityof shortening of a muscle fiber increases with increasing preload. Whena myocardial region contracts late relative to other regions, thecontraction of those opposing regions stretches the later contractingregion and increases the preload. The degree of tension or stress on aheart muscle fiber as it contracts is termed the afterload. Becausepressure within the ventricles rises rapidly from a diastolic to asystolic value as blood is pumped out into the aorta and pulmonaryarteries, the part of the ventricle that first contracts due to anexcitatory stimulation pulse does so against a lower afterload than doesa part of the ventricle contracting later. Thus a myocardial regionwhich contracts later than other regions is subjected to both anincreased preload and afterload. This situation is created frequently bythe ventricular conduction delays associated with heart failure andventricular dysfunction due to an MI. The increased wall stress to thelate-activating myocardial regions is most probably the trigger forventricular remodeling. By pacing one or more sites in a ventricle nearthe infarcted region in a manner which may cause a more coordinatedcontraction, CRT provides pre-excitation of myocardial regions whichwould otherwise be activated later during systole and experienceincreased wall stress. The pre-excitation of the remodeled regionrelative to other regions unloads the region from mechanical stress andallows reversal or prevention of remodeling to occur.

Cardioversion, an electrical shock delivered to the heart synchronouslywith the QRS complex, and defibrillation, an electrical shock deliveredwithout synchronization to the QRS complex, can be used to terminatemost tachyarrhythmias. The electric shock terminates the tachyarrhythmiaby simultaneously depolarizing the myocardium and rendering itrefractory. A class of CRM devices known as an implantable cardioverterdefibrillator (ICD) provides this kind of therapy by delivering a shockpulse to the heart when the device detects tachyarrhythmias. Anothertype of electrical therapy for tachycardia is anti-tachycardia pacing(ATP). In ventricular ATP, the ventricles are competitively paced withone or more pacing pulses in an effort to interrupt the reentrantcircuit causing the tachycardia. Modern ICDs typically have ATPcapability, and deliver ATP therapy or a shock pulse when atachyarrhythmia is detected.

One of ordinary skill in the art will understand that, the modules andother circuitry shown and described herein can be implemented usingsoftware, hardware, and combinations of software and hardware. As such,the terms module and circuitry, for example, are intended to encompasssoftware implementations, hardware implementations, and software andhardware implementations.

The methods illustrated in this disclosure are not intended to beexclusive of other methods within the scope of the present subjectmatter. Those of ordinary skill in the art will understand, upon readingand comprehending this disclosure, other methods within the scope of thepresent subject matter. The above-identified embodiments, and portionsof the illustrated embodiments, are not necessarily mutually exclusive.These embodiments, or portions thereof, can be combined. In variousembodiments, the methods are implemented using a computer data signalembodied in a carrier wave or propagated signal, that represents asequence of instructions which, when executed by one or more processorscause the processor(s) to perform the respective method. In variousembodiments, the methods are implemented as a set of instructionscontained on a computer-accessible medium capable of directing aprocessor to perform the respective method. In various embodiments, themedium is a magnetic medium, an electronic medium, or an optical medium.

The above detailed description is intended to be illustrative, and notrestrictive. Other embodiments will be apparent to those of skill in theart upon reading and understanding the above description. The scope ofthe invention should, therefore, be determined with reference to theappended claims, along with the full scope of equivalents to which suchclaims are entitled.

1. A system, comprising: a lead having a distal end and a proximal end,wherein the distal end includes a plurality of electrodes, and the leadis configured to be fed into a dorsal epidural space of a human to adesired region of a spinal column and to be fed laterally to at leastpartially encircle a spinal cord in the desired region to place at leastone stimulation electrode in position to stimulate a dorsal nerve rootand at least another stimulation electrode in position to stimulate aventral nerve root.
 2. The system of claim 1, further comprising a leadbody extending from the proximal end to the distal end, and a pluralityof conductors for use to selectively deliver stimulation pulses tovarious combinations of the plurality of the electrodes.
 3. The systemof claim 1, further comprising a steerable catheter adapted to beinserted through an introducer into the dorsal epidural space, to be fedvertically up the dorsal epidural space to the desired region, and to befed laterally at least partially around the spinal cord, and wherein thesteerable catheter has a lumen configured to receive and direct the leadto the desired region and at least partially around the spinal cord. 4.The system of claim 1, wherein the lead is a steerable lead adapted tobe fed vertically up the dorsal epidural space to the desired region andto be oriented to be fed laterally at least partially around the spinalcord.
 5. The system of claim 1, wherein: the lead is configured to beset to operationally position at least the first stimulation electrodein a fixated position to stimulate the dorsal nerve root and at leastthe second stimulation electrode in a fixated position to stimulate theventral nerve root; and the proximal end of the lead includes apositional fixation apparatus adapted to maintain a shape and positionof the distal end of the lead.
 6. The system of claim 5, wherein thedistal portion of the lead is made from a material with a predeterminedshape memory predetermined to contract around at least a portion of thespinal column to set the lead.
 7. The system of claim 5, wherein thelead includes a guy wire used to contract the distal portion around atleast a portion of the spinal column to set the lead.
 8. The system ofclaim 1, wherein the plurality of electrodes are configured to direct adirectional stimulation field toward a neural target.
 9. The system ofclaim 1, wherein the plurality of electrodes include ring electrodescircumscribing a circumference of the distal portion of the lead. 10.The system of claim 1, wherein the lead further includes anaccelerometer.
 11. The system of claim 1, further comprising: at leastone switch to select from at least two possible combinations ofstimulation electrodes from the plurality of electrodes; a pulsegenerator adapted to generate neural stimulation pulses, and transmitthe neural stimulation pulses using the lead to a selected combinationof stimulation electrodes; and a controller adapted to: monitor at leastone feedback parameter indicative of efficacious neural stimulation toverify capture of a desired neural target in the dorsal nerve root orthe ventral nerve root or at least one feedback parameter indicative ofan undesired side effect of neural stimulation; and control the at leastone switch to automatically adjust a neural stimulation vector based onthe monitored feedback parameter or a stimulation intensity based on themonitored feedback parameter.
 12. A method for implanting a spinal cordstimulation lead, comprising: introducing the lead into a dorsalepidural space; feeding the lead through the dorsal epidural spaceproximate to a desired vertebra; passing the lead proximate to a dorsalnerve root and a ventral nerve root, wherein passing the lead includes:positioning at least one electrode operationally proximate to the dorsalnerve root to capture at least a portion of the dorsal nerve root withelectrical stimulation delivered using the at least one electrode; andpositioning at least another electrode operationally proximate to theventral nerve root to capture at least a portion of the ventral nerveroot with electrical stimulation delivered using the at least anotherelectrode.
 13. The method of claim 12, further comprising testing animplanted lead position to verify capture.
 14. The method of claim 12,further comprising testing an implanted lead position to abate a sideeffect of the electrical stimulation.
 15. The method of claim 12,wherein the lead is a steerable lead, and passing the lead includessteering the lead to pass proximate to the dorsal nerve root and theventral nerve root.
 16. The method of claim 12, further comprisingsetting the position of the lead.
 17. The method of claim 16, wherein:the lead has a distal end made with a material having shape memory, andthe distal end is made with a predetermined shape to at least partiallysurround the spinal cord; passing the lead includes passing the distalend proximate to the dorsal nerve root and the ventral nerve root whenthe distal end is in a flexed position; and setting the position of thelead includes relaxing the distal end to allow the distal end to atleast partially surround the spinal cord.
 18. The method of claim 17,further comprising: feeding a steerable catheter through the dorsalepidural space and laterally past the desired vertebra and the dorsalnerve root, wherein the catheter includes a lumen extending from aproximal end to a distal end, wherein the lumen is adapted to hold thelead; passing the distal end proximate to the dorsal nerve root and theventral nerve root when the distal end is in a flexed position includespassing the distal end past the dorsal nerve in the catheter; andrelaxing the distal end to allow the distal end to at least partiallysurround the spinal cord includes extending the distal end of the leadout of the distal end of the catheter.
 19. The method of claim 12,wherein: the lead is a steerable lead with at least one steering tendonused to move a distal end of the lead; passing the lead includes movingthe at least one steering tendon to steer the lead past the dorsal nerveroot and the ventral nerve root; and setting the lead includes movingthe at least one steering tendon to at least partially wrap the distalend of the lead around the spinal cord.
 20. The method of claim 12,further comprising: determining whether the lead operably positionselectrodes to successfully capture the ventral nerve root or the dorsalnerve root; adjusting a stimulation field if it is determined that thelead is not operably positioned to successfully capture the ventralnerve root or the dorsal nerve root; and connecting a proximal end ofthe lead to a chronically implanted device if it is determined that thelead is operably positioned to successfully capture the ventral nerveroot or the dorsal nerve root.
 21. The method of claim 20, whereinadjusting the stimulation field includes physically repositioning thelead.
 22. The method of claim 20, wherein adjusting the stimulationfield includes electronically adjusting a stimulation vector.
 23. Themethod of claim 22, wherein electronically adjusting stimulation vectorsincludes selecting at least one different electrode for use instimulating the ventral nerve root or the dorsal nerve root.
 24. Asystem, comprising: means for vertically feeding a lead through a dorsalepidural space proximate to a desired vertebra, and laterally passingthe lead proximate to a dorsal nerve root and a ventral nerve root; andmeans for fixing the lead in position to operatationally place at leastone electrode in position to stimulate at least one of a dorsal nerveroot or a ventral nerve root.
 25. The system of claim 24, furthercomprising: means for stimulating the at least one of the dorsal nerveroot or the ventral nerve root; and means for verifying efficacy of thestimulation.